MLT GlobeBasic Pathology: Hemodynamic disorders – page 7
153 Basic Pathology MCQs on Hemodynamic disorders with answers and explanations.
Amniotic fluid enters the maternal circulation mainly through:
Amniotic fluid embolism occurs when amniotic fluid gains access to maternal venous blood via torn placental membranes or ruptured uterine veins, usually during labour.
Which condition predisposes to left ventricular mural thrombi through dyskinetic wall motion and endocardial damage?
After myocardial infarction, akinetic or dyskinetic myocardium and endocardial injury favour mural thrombus formation, a common source of systemic emboli.
Which of the following would NOT be classified as an embolus?
An embolus must be detached and carried in the blood; it may be solid, liquid or gaseous. A thrombus remaining at its origin is not an embolus.
In the Roman-numeral scheme of coagulation factors, which number is no longer assigned to a distinct factor?
Factor VI was found to be activated factor V and is not used. Factor IV is calcium, factor IX is Christmas factor, factor XIII is fibrin-stabilising factor.
Generalised subcutaneous oedema, especially periorbital, in a patient with heavy proteinuria most likely signals:
Nephrotic syndrome causes albumin loss, reduced oncotic pressure and generalised oedema, often first around the eyes. Subcutaneous oedema also signals heart failure.
During labour a woman suddenly develops severe dyspnoea, cyanosis and hypotension, followed by seizures, coma and DIC. The most likely diagnosis is:
Amniotic fluid embolism presents abruptly during or after labour with respiratory distress, shock, seizures and DIC; mortality is high.
In decompression sickness, gas bubbles in the pulmonary vessels cause oedema, haemorrhage and atelectasis with respiratory distress. This is called:
Pulmonary involvement in decompression sickness is known as the chokes; musculoskeletal pain is the bends.
In chronic passive congestion of the lung, the alveolar septa become:
Chronic pulmonary congestion causes septal thickening, fibrosis and haemosiderin-laden macrophages ('heart failure cells'), producing brown induration.
In acute congestion of the liver, which structures are distended with blood?
Acute hepatic congestion distends the central veins and sinusoids; hepatocytes may undergo centrilobular ischaemic injury.
The hypotension and vasodilation of septic shock are driven mainly by which host mediators released in response to microbial products?
Microbial components (e.g. LPS) activate innate immune cells to release TNF, IL-1 and other cytokines that cause vasodilation, endothelial activation and DIC. IgE-mediated release underlies anaphylaxis, not sepsis.
Over the days after arterial occlusion in the kidney, a pale (white) infarct changes grossly by becoming:
Pale infarcts in solid organs with end-arterial supply become progressively paler and better defined as a hyperaemic border forms. Poorly defined red lesions are typical of haemorrhagic infarcts.
In a patient in progressive shock, which laboratory finding best reflects cellular hypoperfusion?
Hypoperfused cells switch to anaerobic glycolysis, producing lactic acid; rising lactate indicates tissue hypoperfusion and worsening prognosis. Alkalosis and high albumin are not features.
A patient develops hypotension with bradycardia and warm skin after an acute cervical spinal cord injury. This is best classified as:
Loss of sympathetic vascular tone after spinal cord or brain injury causes vasodilation and pooling of blood: neurogenic shock. Bradycardia distinguishes it from hypovolaemic shock.
In early septic shock, cardiac output may be normal or high, yet tissues remain hypoperfused mainly because of:
Mediators such as nitric oxide and cytokines cause systemic vasodilation, lowering vascular resistance and pooling blood, so tissues are underperfused despite adequate output.
According to current data, septic shock is most frequently triggered by infection with:
Gram-positive bacterial infections are now the most common trigger of septic shock, followed by gram-negative bacteria and fungi.
Which statement best describes the initial (non-progressive) stage of shock?
In the non-progressive stage, catecholamines, RAAS activation and ADH maintain perfusion of vital organs; with treatment it is fully reversible. The other options describe later stages.
Under the current (Sepsis-3) definition, sepsis is:
Sepsis-3 (2016) defines sepsis as organ dysfunction caused by a dysregulated host response to infection; SIRS criteria alone are no longer used to define it. Bacteraemia alone is not sepsis.
Toxic shock syndrome, caused by secreted staphylococcal or streptococcal proteins, most closely resembles which condition?
Superantigen-driven cytokine release produces fever, rash, vasodilation, hypotension and multi-organ failure, a picture similar to septic shock. It is not IgE-mediated or due to pump failure.
Which type of shock is the leading cause of death in non-coronary intensive care units?
Septic shock is the commonest cause of death in non-coronary ICUs and carries mortality of about 20–30% even with treatment.
Gram-negative lipopolysaccharide triggers the inflammatory cascade of sepsis mainly by binding which receptor on macrophages?
LPS, with LBP and CD14, signals through TLR4 to activate NF-κB and release TNF, IL-1 and other cytokines. Fc epsilon receptors bind IgE.